From the Archives
‘Visual field changes following anterior temporal lobectomy: their significance in relation to "Meyer's loop" of the optic radiation.’ By Murray A. Falconer and John L. Wilson (From the Guy's-Maudsley Neurosurgical Unit, London). Brain 1958; 81: 1–14 and ‘The architecture of the optic radiation in the temporal lobe of man. By J. M. van Buren and M. Baldwin (From the Branch of Surgical Neurology, National Institute of Neurological Diseases and Blindness, National Institutes of Health, Public Health Service, US Department of Health, Education, and Welfare). Brain 1958; 81: 15–40.In his paper on field defects produced by temporal lobe lesions (H. Cushing, Distortions of the visual fields in cases of brain tumour: the field defects produced by temporal lobe lesions. Brain 1922; 44: 371–96), Harvey Cushing recalls the occasion at Johns Hopkins Hospital in October 1910 when a patient with epilepsy resulting from gunshot injury, in which the ball had penetrated the left eye and lodged in the temporal lobe on that side, was mistakenly considered to have normal vision in the remaining right eye by the painstaking house officer (Dr S. J. Crowe). Dr Adolf Meyer happened to visit the ward and suggested that a sector shaped defect might be detected if the field was to be plotted at <30° intervals; and he was correct (Fig. 1). Three years earlier, Dr Meyer's paper (A. Meyer, The connections of the occipital lobes and the present status of the cerebral visual affections. Transactions of the Association of American Physicians 1907; 22: 7–16), which Cushing considered to have received an undeserved lack of attention, had described ‘the peculiar detour of the ventral portion of the geniculocalcarine path’. By studying secondary degenerations following vascular or traumatic lesions, Meyer had concluded that a portion of the optic radiation, on leaving the geniculate body, plunges forward into the temporal lobe to sweep around the horn of the ventricle before it turns backwards to end in the calcarine cortex. The dorsolateral and ventral bundles of the tract remain the same size throughout and maintain definite positions in relation to other bundles. Thus, the dorsolateral bundle takes the more direct route from the geniculate body, whereas the most ventral bundles make the longest detour around the temporal horn eventually ending in the anterior part of the calcarine cortex. At the request of Dr Meyer, the distinguished medical artist Max Brodel created a glass model of the optic radiation, that Cushing considered ‘renders superfluous any further written description’, 2D images of which were much reproduced (Fig. 2). Although Meyer had not supplemented his original anatomical observations with perimetry, shrewdly he had surmised that the dorsal bundles provide upper retinotopic representation and their damage, therefore, would result in lower quadrantic field defects, whereas involvement of the ventral bundles should be associated with defects in the upper quadrant; this, the luckless Dr Crowe had failed to detect. But the anatomical details of Meyer's loop, and the exact field defects to be expected when it is damaged, were not so readily agreed.
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Murray Falconer and John Wilson line up contrary opinions from the literature, based on the analysis of tumour cases and gunshot wounds, as the basis for considering whether or not the homonymous field defects of temporal lobe lesions are confined to the upper field, and are invariably congruous in the two eyes. With John van Buren and Maitland Baldwin, they argue the case for an improved understanding of these matters through the study of cases in which the damage to ‘Meyer's loop’ is not confounded by diffuse tissue injury resulting from tumour or gunshot injury. Their context is temporal lobectomy for the treatment of epilepsy.
Falconer and Wilson analyse 50 consecutive cases in whom temporal lobectomy invariably involved opening up the temporal horn of the lateral ventricle and removal of the anterior portion of the hippocampus (Ammon's horn), the uncus and the amygdala. Using quantitative perimetry, field defects could be detected in all cases. The hemianopia starts in the upper field at the vertical meridian and, with increasing damage to the visual pathway, extends in sectors towards the horizontal boundary of the upper quadrant. At first, the lower margin slopes down to the point of fixation but, with time, this assumes the horizontal. The macula is spared until the defect enters the lower quadrant. For Falconer and Wilson, the hemianopic defects are invariably congruous. Together, the findings support Adolf Meyer's anatomical conclusions. Variations in the extent of the homonymous defect depend on the degree of anterior sweep in Meyer's loop and variable size of the temporal lobe. Since an incision running parallel to fibres of the optic radiation does not cut across additional layers of the loop, resections between 4.5 and 8 cm produce equivalent field defects. Much beyond 8 cm, parts of the optic radiation starting to pass obliquely beneath the ventricle are cut and the defect extends.
For van Buren and Baldwin, the architecture of the optic radiation in the temporal lobe has gained a spurious authority through reproduction of Cushing's appealing diagram (Fig. 2). Condemning thus with faint praise, they point out that physiological evidence based on visual field examination in man challenges the dogma. Unlike Falconer and Wilson, their surgical technique strove not to enter the ventricular system at the temporal horn but this precision was not always possible when epileptic activity was shown to originate from deeper recesses of the temporal lobe. In five cases, the tip of the temporal ventricular horn had been opened but without causing a field defect. Perimetry was not performed until the patient could tolerate examination lasting 45 min—generally at around 14 days after surgery. Their series consists of 41 cases. Visual acuity is always preserved. Field loss most closely approaches the point of fixation in the upper vertical meridian. The temporal monocular crescent is lost beyond a sector defect in the upper field. Characteristically, the horizontal meridian bows up towards the point of fixation, the more medial boundary most usually assuming the horizontal, producing a sector shaped defect: its contour may flatten if a second surgical procedure is required but the overall area of field loss does not increase. Sometimes, the defect straddles the horizontal meridian, especially when smaller isopters are mapped. Conversely, apparent crossing of the vertical meridian does not occur and, when claimed, is explained by head tilt—thus rotating the field—or because ‘there are so few straight lines in Nature’. Unlike Falconer and Wilson, the majority of patients (23 of 33 with demonstrable field defects) show lack of congruity in the homonymous quadrantinopia. The larger defect most nearly approaches the fixation point and is always to be found in the eye on the side of the temporal lobectomy. Despite differences in size, the slope of the lower margin is identical in the two eyes. The macula is spared because fibres subserving central vision lie in the medial aspect of the radiation, whereas those concerned with peripheral vision lie more lateral and, hence, are especially vulnerable to surgical resection.
van Buren and Baldwin are not shy in challenging the writings of Cushing and (Sir) Gordon Holmes on the neurology of field defects after temporal lobe lesions. They conclude that no one should be surprised by intact visual acuity; nor invariable loss of the monocular temporal crescent odd, at least in the context of damage to the anterior part of the optic radiation, even though Holmes had described selective loss of central vision in the hemianopic field with cortical lesions. They do not like the explanation offered by Harvey Cushing and Clifford Walker (Distortions of the visual fields in cases of brain tumours: chiasmal lesions, with especial reference to bitemporal hemianopsia. Brain 1915; 37: 341–400) or H.M. (Harry Moss) Traquair (An Introduction to Clinical Perimetry, 1927), who attributed the inferior slope of field defects to ischaemia of juxtaposed tissue or compression by tumours of the nearby optic tract. On the contrary, there must be an anatomical explanation based on distributed retinotopic representation in the radiation itself: ‘all fibres derived from a given retinal point do not lie close together in the optic radiation.’ Cases in which the defect straddles the horizontal meridian indicate the continuity of adjacent radial sectors of the peripheral field without, as Holmes had proposed, these being separated by macular fibres. Those subserving the central field lie medial to fibres representing peripheral vision. On congruity, they disagree profoundly with Traquair who had declared that ‘all hemianopias due to a supra-geniculate lesion must be congruous’. Furthermore, Harvey Cushing's observation that the larger defect may be on either side, is criticized on the basis that, being ill, his patients were not fully able to cooperate, and their examinations not therefore reliable. They correct Gordon Holmes's opinion (Introduction to Clinical Neurology, 1946) that ‘when the radiations are involved it is occasionally incongruous and is then usually greater in the opposite eye in which the temporal field is lost’; again, paying undue attention to cases with tumours had led Sir Gordon astray. Taken together, van Buren and Baldwin argue that the optic radiation does not cap the temporal horn; retinal representation on either side of the vertical meridian lies farthest forward and therefore, makes the largest excursion into the temporal lobe; anterior placed lesions are most likely to catch the anterior looping fibres and so produce paravertical field defects; but, as the lesion extends to the posterior and inferior limits, the lower border will change its angle from oblique to horizontal with respect to the point of fixation; a lesion advancing from the lateral aspect of the radiation will injure ipsilateral more than contralateral retinal fibres resulting in non-congruous defects with a larger area of loss on the side of the lesion; conversely, a lesion advancing from the anterior aspect of the radiation will injure fibres from each eye to the same degree causing a congruous defect (Fig. 3).
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In revisiting the functional anatomy of the optic radiation within the temporal lobe, Jason Barton and colleagues (page 2123) bring Meyer's loop full circle—or at least rotate it through 90o.
Cambridge, UK
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